» Articles » PMID: 32867388

Neuroprotective Properties of Green Tea () in Parkinson's Disease: A Review

Overview
Journal Molecules
Publisher MDPI
Specialty Biology
Date 2020 Sep 2
PMID 32867388
Citations 29
Authors
Affiliations
Soon will be listed here.
Abstract

Neurodegenerative disease is a collective term given for the clinical condition, which results in progressive degeneration of neurons and the loss of functions associated with the affected brain region. Apart from the increase in age, neurodegenerative diseases are also partly affected by diet and lifestyle practices. Parkinson's disease (PD) is a slow onset neurodegenerative disorder and the second most common neurodegenerative disease, which affects the motor system. Although there is no prescribed treatment method to prevent and cure PD, clinical procedures help manage the disease symptoms. Green tea polyphenols are known for several health benefits, including antioxidant, anti-inflammatory, and neuroprotective activity. The current manuscript summarizes the possible mechanisms of neuroprotective potential of green tea with a special focus on PD. Studies have suggested that the consumption of green tea protects against free-radicals, inflammation, and neuro-damages. Several in vivo studies aid in understanding the overall mechanism of green tea. However, the same dose may not be sufficient in humans to elicit similar effects due to complex physiological, social, and cultural development. Future research focused on more clinical trials could identify an optimum dose that could impart maximum health benefits to impart neuroprotection in PD.

Citing Articles

NaCTR: Natural product-derived compound-based drug discovery pipeline from traditional oriental medicine by search space reduction.

Jung S, Kim K, Wang S, Han M, Lee D Comput Struct Biotechnol J. 2024; 23:3869-3877.

PMID: 39554615 PMC: 11564001. DOI: 10.1016/j.csbj.2024.10.035.


Neurodegenerative diseases and catechins: (-)-epigallocatechin-3-gallate is a modulator of chronic neuroinflammation and oxidative stress.

Li S, Wang Z, Liu G, Chen M Front Nutr. 2024; 11:1425839.

PMID: 39149548 PMC: 11326534. DOI: 10.3389/fnut.2024.1425839.


Polyphenols: Secondary Metabolites with a Biological Impression.

Bolat E, Saritas S, Duman H, Eker F, Akdasci E, Karav S Nutrients. 2024; 16(15).

PMID: 39125431 PMC: 11314462. DOI: 10.3390/nu16152550.


Gut-Brain Axis in Focus: Polyphenols, Microbiota, and Their Influence on α-Synuclein in Parkinson's Disease.

Riegelman E, Xue K, Wang J, Tang L Nutrients. 2024; 16(13).

PMID: 38999791 PMC: 11243524. DOI: 10.3390/nu16132041.


Role of Epigenetic Modulation in Neurodegenerative Diseases: Implications of Phytochemical Interventions.

Prasanth M, Sivamaruthi B, Cheong C, Verma K, Tencomnao T, Brimson J Antioxidants (Basel). 2024; 13(5).

PMID: 38790711 PMC: 11118909. DOI: 10.3390/antiox13050606.


References
1.
Batista-Nascimento L, Pimentel C, Menezes R, Rodrigues-Pousada C . Iron and neurodegeneration: from cellular homeostasis to disease. Oxid Med Cell Longev. 2012; 2012:128647. PMC: 3369498. DOI: 10.1155/2012/128647. View

2.
Cooper J, Sagar H, Jordan N, Harvey N, Sullivan E . Cognitive impairment in early, untreated Parkinson's disease and its relationship to motor disability. Brain. 1991; 114 ( Pt 5):2095-122. DOI: 10.1093/brain/114.5.2095. View

3.
Devi L, Raghavendran V, Prabhu B, Avadhani N, Anandatheerthavarada H . Mitochondrial import and accumulation of alpha-synuclein impair complex I in human dopaminergic neuronal cultures and Parkinson disease brain. J Biol Chem. 2008; 283(14):9089-100. PMC: 2431021. DOI: 10.1074/jbc.M710012200. View

4.
Cuervo A, Stefanis L, Fredenburg R, Lansbury P, Sulzer D . Impaired degradation of mutant alpha-synuclein by chaperone-mediated autophagy. Science. 2004; 305(5688):1292-5. DOI: 10.1126/science.1101738. View

5.
Przedborski S, Kostic V, Jackson-Lewis V, Naini A, Simonetti S, Fahn S . Transgenic mice with increased Cu/Zn-superoxide dismutase activity are resistant to N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity. J Neurosci. 1992; 12(5):1658-67. PMC: 6575882. View